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The Pharmaceutical Journal
Vol 268 No 7195 p593
27 April 2002

Veterinary Pharmacists Group

Zoonotic risks in summer months

Zoonoses are infectious animal-associated diseases that may be transmitted to man from vertebrate animals by bites, scratches, injection of saliva from ectoparasites, and inhalation of airborne agents. The definition includes human diseases acquired from animals and those produced by non-infective agents (eg, toxins and poisons). Strictly speaking, the definition excludes ectoparasites, which act as intermediate hosts and can both transmit zoonotic diseases and cause them from allergic reactions or bites.

The interaction of agent, host and the external environment determines the degree of susceptibility of the host to infection and the subsequent development of the disease. Carrier hosts and asymptomatic infected individuals are important in the persistence of many zoonotic agents. The infecting agent persists in nature (zoonotic reservoirs) in vertebrate animals.

The most spectacular implication of zoonoses in modern times has been associated with the spread of AIDS. Researchers have shown that HIV-1 and HIV-2 were introduced into the human population by zoonotic cross-species transmission of the Simian immunodeficiency virus (SIV) from chimpanzees1 and sooty mangabeys,2 respectively. These zoonotic transmissions probably occurred in the course of butchering apes for food.3 However, it is unclear exactly what set off the life threatening AIDS epidemic in the late 1970s after an extended period during which apparently "peaceful" co-existence between humans and HIV had occurred in many isolated communities in Central Africa.4 It is fully acknowledged that we do not have such direct and serious sources of animal infection in this country but during the summer months two zoonotic risks associated with pet ownership become more visible in the United Kingdom.

Lyme disease

Imagine that you are faced with a client seeking advice about a swollen elbow. Golfers' elbow? A knock? Arthritis? When all these have been eliminated from the enquiry as a possible explanation, what next? Well at this time of year it is just possible that one could be faced with a case of Lyme disease.

Lyme disease is a systemic tick-borne disease with many clinical symptoms.5 Although rarely fatal, the disease can be long-term and debilitating with cardiac, neurologic and joint involvement. Initial symptoms may include 'flu-like symptoms with headache, stiff neck, myalgia, malaise and low grade fever. A circular painless macular dermatitis may be present at the site of the bite. Joint swelling may be present and is often what prompts action.

The story of the recognition of Lyme disease is interesting. In 1975 a geographic cluster of children in a small America community at Lyme presented with what appeared to be juvenile arthritis. The spirochete causing the disease, subsequently named Borrelia burgdorferi, was not identified until 1982. The natural disease reservoirs are thought to be wild deer, rodents and associated ticks, Ixodes ricinus. Other species of tick are responsible in America, where the disease is endemic in many regions. In the UK, the great parks of southern England are likely habitats.

Human infection is acquired from tick bites, although in many cases, the individual may not remember being bitten. Dogs also suffer from the disease, which can manifest itself as chronic arthritis.

Hard ticks have four developmental stages: egg, larva, nymph and adult. Each of the three motile stages must attach to a host, feed, fall off and then transform into the next stage. If no blood-providing host is available the ticks perish.

Early stage Lyme disease responds readily to oral antibiotics such as amoxicillin or doxycycline, prescribed for two to three weeks. Late stage treatment is considerably more difficult; intravenous antibiotics are often used.

It is certainly worthwhile asking likely patients if they have been in forest areas frequented by wild deer and if they remember being bitten while walking in long grass. Referral to the GP might be met with scepticism, but it is worth persevering. More and more cases are being seen in England, so pharmacists should not be surprised to encounter an example.


Another problem during the warmer summer months is associated with ectoparasites. Control of fleas and related organisms is important because they can pose a zoonotic risk and act as vectors in the transmission of disease. They often present quite a problem.6

Fleas breed in warm weather, and the pupas hatch simultaneously when stimulated by vibration (which equals good news to fleas, indicating that there is a meal about). So, on return from holiday, a room that has been the favoured snoozing place for pets can suddenly appear be alive with infestation.7

The most usual clinical signs in cats and dogs are scratching, pruritis and skin conditions brought on by hypersensitivity to flea saliva during the warmer months. In some cases a cat living in the same household as a dog may provide a reservoir of fleas for the latter, but is unaffected itself. The main source of the dried blood necessary for larval development is the adult parasite faeces, often present in the bedding.

To obtain effective control, both the animal and its surroundings must be treated. Products to treat infestation are readily available from pharmaceutical wholesalers. Topical sprays are the most popular form of medication, probably because of their ease of use, followed by powders. Collars are also useful, but although they provide insecticidal protection, their continual contact with the skin can invoke an allergic reaction.

In recent years resistant "super fleas" have appeared across southern England and clients with allergic reactions from bites may well present in the pharmacy.8

? Steven Kayne, VPG committee member


1. Gao F, Bailes E, Robertson DL, Chen Y, Rodenburg CM, Michael SF, Cummins LB, Arthur LO, Peeters M, Shaw GM, Sharp PM, Hahn BH. Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes. Nature 1999;397:436? 41.

2. Chen Z, Luckay A, Sodora DL, Telfer P, Reed P, Gettie A, Kanu JM, Sadek RF, Yee J, Ho DD, Zhang L, Marx PA. Human immunodeficiency virus type 2 (HIV-2) seroprevalence and characterization of a distinct HIV-2 genetic subtype from the natural range of simian immunodeficiency virus-infected sooty mangabeys. J Virol 1997;71(5): 3953?60.

3. Chitnis A, Rawls D, Moore J. Origin of HIV Type 1 in colonial French Equatorial Africa. AIDS Res Hum Retroviruses 2000;16:5?8.

4. Hrdy DH. Cultural practices contributing to the transmission of himan immunodeficiency virus in Africa? Rev Infect Dis 1987;9: 1109? 15.

5. O'Connell S. Fortnightly review: Lyme disease in the United Kingdom BMJ 1995;310:303?8.

6. Currey J. Come back DDT ? all is forgiven. BMJ 1994;309:1692

7. Williamson B. Eradicating fleas (Letter). BMJ 1995;310:672.

8. Kayne SB. Fleas (Letter). Pharm J 1995:255:72.

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